Rapid neurology and neurosurgery 9780470654439, 0470654430

Table of contents :
Content: pt. 1. The basics --
pt. 2. Complaints : face-to-face with the patient --
pt. 3. Conditions : applying the basics.

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Rapid Neurology and Neurosurgery

Rapid Neurology and Neurosurgery Kumar Abhinav BSc (Hons.), MBBS, MRCS (Eng) Specialty Registrar Department of Neurosurgery Frenchay Hospital Bristol, UK

Richard Edwards BSc (Hons.), MBBS, FRCS (Neuro.Surg), MD Consultant Neurosurgeon & Senior Clinical Lecturer (University of Bristol) Department of Neurosurgery Frenchay Hospital Bristol, UK

Alan Whone MBChB, MRCP, PhD Senior Lecturer (University of Bristol) & Consultant Neurologist Department of Neurology Frenchay Hospital Bristol, UK

This edition first published 2012 # 2012 by John Wiley & Sons, Ltd Wiley-Blackwell is an imprint of John Wiley & Sons, formed by the merger of Wiley’s global Scientific, Technical and Medical business with Blackwell Publishing. Registered office: John Wiley & Sons, Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK Editorial offices: 9600 Garsington Road, Oxford, OX4 2DQ, UK The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK 111 River Street, Hoboken, NJ 07030-5774, USA For details of our global editorial offices, for customer services and for information about how to apply for permission to reuse the copyright material in this book please see our website at www.wiley.com/wiley-blackwell. The right of the author to be identified as the author of this work has been asserted in accordance with the UK Copyright, Designs and Patents Act 1988. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior permission of the publisher. Designations used by companies to distinguish their products are often claimed as trademarks. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respective owners. The publisher is not associated with any product or vendor mentioned in this book. This publication is designed to provide accurate and authoritative information in regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged in rendering professional services. If professional advice or other expert assistance is required, the services of a competent professional should be sought. Library of Congress Cataloging-in-Publication Data Abhinav, Kumar. Rapid neurology and neurosurgery / Kumar Abhinav, Richard Edwards, Alan Whone. p. ; cm. – (Rapid series) Includes bibliographical references and index. ISBN 978-0-470-65443-9 (pbk. :alk. paper) I. Edwards, Richard (Richard John) II. Whone, Alan. III. Title. IV. Series: Rapid series. [DNLM: 1. Nervous System Diseases–Handbooks. 2. Neurosurgical Procedures–Handbooks. 3. Trauma, Nervous System–Handbooks. WL 39] 616.80076–dc23 2012009836 A catalogue record for this book is available from the British Library. Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books. Cover image: iStock # Sebastian Kaulitzki Cover design by Fortiori Design Set in 7.5/9.5pt Frutiger-Light by Thomson Digital, Noida, India

1 2012

Contents List of Abbreviations, vii Preface, xi Acknowledgements, xiii

PART I The basics 1

About this book and how to use it, 3

2

Basic neuroanatomy, 4

3

Neurological history, examination, signs and localisation, 7

4

Neurological investigations, 21

PART II Complaints: Face-to-face with the patient 5

Headache, 31

6

Blackouts, 34

7

Visual disturbances, 36

8

Dizziness and vertigo, 39

9

Weak legs, 41

10 Numbness and sensory disturbance, 44 11 Gait assessment and disturbance, 46

PART III Conditions: Applying the basics 12 Headache, 51 13 Transient ischaemic attacks (TIAs), 55 14 Stroke I: Thromboembolic stroke and syndromes, 59 15 Stroke II: Intracerebral haemorrhage, 65 16 Stroke III: Subarachnoid haemorrhage, 68 17 Epilepsy, 75 18 Multiple sclerosis, 80 19 Parkinson’s disease and other related syndromes, 84 20 Other movement disorders, 88 21 Central nervous system infections: Meningitis, 91 22 Central nervous system infections: Cerebral abscess, 94 23 Radiculopathy and disc herniation, 97 24 Peripheral neuropathies’ syndromes, 100 25 Common peripheral nerve lesions: Mononeuropathies, 104 26 Motor neurone disease (MND), 108 27 Myasthenia gravis and Lambert–Eaton myasthenic syndrome, 111 28 Diseases of the muscle, 114 29 Alzheimer’s disease and other dementia syndromes, 118 30 Raised intracranial pressure and herniation syndromes, 122 31 Coma and brainstem death, 127

vi

Contents

32 Head injury: General approach and management, 130 33 Head injury: Subdural haematoma, skull fractures and contusions, 135 34 Head injury: Extradural haematoma, 141 35 Spinal injuries and spinal cord syndromes, 144 36 CNS neoplasia, 151 37 Hydrocephalus, 155

Appendices Appendix 1 Management of status epilepticus (SE), 163 Appendix 2 Glasgow Coma Scale (GCS), 164 Appendix 3 Primary neuroepithelial tumours of the central nervous system, 166 Appendix 4 Other tumours affecting the central nervous system, 173

Index, 181

List of Abbreviations ABC AD ADEM ADHD AED AF ALS APP ASDH AVMs BNF BPV CAA CADASIL

CBF CES CIDP CMAP CN CNS CPP CSDH CT CTA CTS CVR DAI DBS DIND DVLA DVT EEG EMG EMQ ET ETV EVD FTD

Airways and breathing and circulation Alzheimer’s disease Acute disseminated encephalomyelitis Attention deficit hyperactivity disorder Antiepileptic drug Atrial fibrillation Amyotrophic lateral sclerosis Amyloid precursor protein Acute subdural haematoma Arteriovenous malformations British National Formulary Benign positional vertigo Cerebral amyloid angiopathy Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy Cerebral blood flow Cauda equina syndrome Chronic inflammatory demyelinating polyneuropathy Compound muscle action potential Cranial nerve Central nervous system Cerebral perfusion pressure Chronic subdural haematoma Computed tomography CT angiography Carpal tunnel syndrome Cerebral vascular resistance Diffuse axonal injury Deep brain stimulation Delayed ischaemic neurological deficit Driver and Vehicle Licensing Agency Deep venous thrombosis Electroencephalogram Electromyography Extended matching questions Essential tremor Endoscopic third ventriculostomy External ventricular drain Frontotemporal dementia

viii

FVC GCA GBM GBS GCS GTC HACE ICH ICP IIH INO IVIG LACS LEMS LBD LMN LOC LP LP MAP MCI MCQ MDT MG MND MRA MRC MRI MS MUPs NAHI NCS NMJ NPH OCSP OSCE PACS PBP PCC PD PE PEG

List of Abbreviations

Forced vital capacity Giant cell arteritis Glioblastoma multiforme Guillian–Barre syndrome Glasgow Coma Scale Generalised tonic–clonic High altitude cerebral oedema Intracerebral haemorrhage Intracranial pressure Idiopathic intracranial hypertension Internuclear opthalmoplegia Intravenous immunoglobulin Lacunar stroke Lambert–Eaton myasthenic syndrome Lewy body dementia Lower motor neurone Loss of consciousness Lumbar puncture Lumboperitoneal Mean arterial pressure Mild cognitive impairment Multiple choice questions Multidisciplinary team Myasthenia gravis Motor neurone disease MR angiography Medical Research Council Magnetic Resonance Imaging Multiple sclerosis Motor unit potentials Non-accidental head injury Nerve conduction studies Neuromuscular junction Normal pressure hydrocephalus Oxford Community Stroke Project Objective Structured Clinical Examinations Partial anterior circulation stroke Progressive bulbar palsy Prothrombin complex concentrate Parkinson’s disease Pulmonary embolism Percutaneous endoscopic gastrostomy

List of Abbreviations

PFO PLS PMA PNS POCS PPMS PRES PTA RAPD RAS REZ RRMS RTA SACD SAH SCI SCM SE SEM SPMS TACS TBI TIAs TN UMN VA VP

Patent foramen ovale Primary lateral sclerosis Progressive muscular atrophy Peripheral nervous system Posterior circulation stroke Primary progressive multiple sclerosis Posterior reversible encephalopathy syndrome Posttraumatic amnesia Relative afferent pupillary defect Reticular activating system Root entry zone Relapsing/remitting multiple sclerosis Road traffic accidents Subacute combined degeneration of the cord Subarachnoid haemorrhage Spinal cord injury Sternocleidomastoid Status epilepticus Spinal extradural metastases Secondary progressive multiple sclerosis Total anterior circulation stroke Traumatic brain injury Transient ischaemic attacks Trigeminal neuralgia Upper motor neurone Ventriculoatrial Ventriculoperitoneal

ix

Preface My late grandfather, a university professor, used to talk about the so-called ‘ideal’ students, who read extensively on a topic prior to attending the relevant lecture, made their own ‘notes’ in their own ‘words’ in a summarised fashion, which they subsequently memorised in the lead up to the exams. This inspirational philosophy with respect to teaching and the ‘ideal’ learning method can be difficult to adhere to as a modern medical student, where the ever-increasing breadth of the curriculum makes it difficult to both identify the pertinent information and then assimilate it in preparation for the exams. Our objective was to put together a book in a condensed format, which gave the necessary basic information for building a solid foundation in neurology and neurosurgery required by medical students and junior doctors, and then followed it up with sections on presenting complaints and all the key clinical conditions. This book aims to simplify information in specialties traditionally considered ‘difficult’, to which medical students have variable and usually limited exposure, and to facilitate focused exam preparation. We really hope differential diagnoses tables, a consistent feature across this book, are helpful particularly for OSCE and EMQ sections of the exam and are used to refresh knowledge from other cross-referenced chapters during revision. We sincerely hope this easy-to-use and concise book with ample practical information is useful for exams and as a reference guide on the wards and clinics for medical students, junior doctors and other health professionals in neurology and neurosurgery. Kumar Abhinav Richard Edwards Alan Whone

Acknowledgements We are indebted to all those who provided helpful advice at different stages of the production of the book. We are also grateful to the medical students and junior doctors who provided invaluable advice regarding improving the contents of the book. Specifically, we would like to acknowledge the following at Frenchay Hospital, Bristol: Mr Kristian Aquilina, Consultant Neurosurgeon for authoring the chapters on meningitis and cerebral abscess; Dr Philip Clatworthy, Specialist registrar in Neurology and Stroke Medicine, for his contribution towards the chapters on transient ischaemic attacks and thromboembolic stroke and syndromes, and Mr Devindra Ramnarine, Senior registrar in Neurosurgery, for his feedback regarding the chapter on radiculopathy and disc herniation. We would further like to thank all our colleagues at the Wiley-Blackwell: in particular, Martin Davies for his support through the initial stages of the book proposal and Laura Murphy for her guidance through the preparation of the manuscript. Finally, we are immensely thankful to our partners and families for their encouragement and patience through the preparation of the book and particularly to Melanie Yoogalingam for her help and support throughout this endeavour.

Part I The basics

ABOUT THIS BOOK AND HOW TO USE IT

1

3

About this book and how to use it

The principal purpose of this book is to act as a quick revision tool for medical students approaching finals or other undergraduate neurology/neurosurgery exams. Although the book is intended as a quick revision tool, using it diligently and devoting time to understanding the basic concepts outlined herein will allow you to neurologically flourish rather than simply pass exams. The book is designed for both the newer type of written exams, including multiple choice questions (MCQ) as well as the extended matching questions (EMQ), and traditional exams requiring long and short answers. This book is also designed to prepare you for the Objective Structured Clinical Examinations (OSCE); in particular, Part II is geared towards this purpose. The book is divided into three parts. Part I gives you the necessary basic principles and facts essential for building a foundation in clinical neurology/neurosurgery at an undergraduate level. Only clinically relevant neuroanatomy is presented along with an introduction to the topics of neurological history, examination and investigations. In particular, we have tried to simplify neuroradiological concepts and presented the rationale for using different imaging modalities. Part II is very much geared towards the OSCE and the viva voce exams in finals. This section consists of chapters dealing with various presenting complaints. Lists of focussed and discriminating questions for determining the important differential diagnoses are included in these chapters along with tables listing the relevant disease entities in order of incidence. Please note, however, that you will also be expected to ask other relevant questions not listed in the chapters while taking a detailed history, including past medical history, drug history and social history. Additional important clinical information for each presenting complaint is included. The tables of potential differential diagnoses are supplemented by information on basic investigations and management. Again, in an exam setting you will have to be guided by the clinical information and suggest a list of focussed and relevant investigations! This part of the book can also act as a worthy quick reference on wards and in clinics. Part III presents the important clinical neurological and neurosurgical conditions with focussed pertinent clinical information. Neurological topics are presented first followed by neurosurgical topics with the exception of the chapter on subarachnoid haemorrhage, which is included under ‘stroke’. Part III like other parts is interspersed with sentences beginning with ‘Remember . . . ’ and designed to highlight key facts from the chapter. At the end of each chapter there is a list of common differential diagnoses (up to a maximum of four–five) for the particular condition described. General clinical details are provided, including, where applicable, information that can be used to distinguish between or exclude the alternative conditions. This should be of particular help for the EMQ section of the exam and will also prove useful in the OSCE when presenting a list of potential differential diagnoses. Some of the chapters in the book may not strictly follow the format as laid out above and will generally be due to the nature of the topic and thereby the limitations of presenting it in a specific format. We hope that the format; organisation and simple language employed will facilitate quick and effective revision and will help you perform well in all sorts of undergraduate examinations. Moreover, we trust this book will permit a better understanding of the basic concepts underpinning neurology and neurosurgery and thus provide a firm basis upon which to build your clinical neurological/neurosurgical expertise as you journey through your medical career. Good Luck!

THE BASICS

4

2

Basic neuroanatomy

The following section aims to present only the very relevant anatomical information.

Cortical anatomy Figure 2.1 demonstrates the following relevant key areas on the cortical surface:  Primary motor cortex: Situated anterior to central sulcus (frontal lobe) in the precentral gyrus; involved in contralateral motor function—Brodmann’s (Br.) Area 4.  Primary somatosensory cortex: Situated posterior to central sulcus (parietal lobe) in the postcentral gyrus; involved in contralateral sensory function—Br. Areas 1, 2 and 3.  Motor speech area: In the dominant hemisphere only (left hemisphere for right-handed subjects and usually left hemisphere for left-handed people); anatomically situated in the inferior frontal gyrus (pars triangularis and opercularis); also known as ‘Broca’s area’ and involved in speech output—Br. Area 44.  Wernicke’s area: In the dominant hemisphere; anatomically situated in the supramarginal gyrus—Br. Area 40 (part of inferior parietal lobule) and posterior part of superior temporal gyrus; involved in comprehension of speech.  Primary visual cortex: In the occipital lobe adjacent to the calcarine sulcus—Br. Area 17; part of the visual pathway. Remember: The association between dominant hemisphere and speech areas and therefore a further important point about ascertaining handedness of patients at the beginning of obtaining a neurological history.

Brainstem and cranial nerves (CN) The midbrain is the most rostral part of the brainstem; CN III (oculomotor) and IV (trochlear) arise from the midbrain. The pons is situated between the midbrain and the medulla with CN V (trigeminal), VI (abducens), VII (facial) and VIII (vestibulocochlear) nerve entering into Central sulcus Precentral gyrus (motor cortex)

Post central gyrus (sensory cortex)

Superior frontal gyrus

Supramarginal gyrus Angular gyrus

Middle frontal gyrus Inferior frontal gyrus

Primary visual cortex (occipital lobe)

Broca’s area (frontal lobe)

Superior temporal gyrus Middle temporal gyrus

Wernicke’s area (may also include posterior superior temporal gryrus)

Inferior temporal gyrus

Sylvian fissure

Primary auditory area

Figure 2.1 Lateral surface of cerebral hemisphere demonstrating cortical surface anatomy.

BASIC NEUROANATOMY

5

or exiting from ventral pons. The medulla is caudal to pons being continuous with spinal cord. Fibres of the CN IX (glossopharyngeal), X (vagus) and XII (hypoglossal) nerves enter into or exit from the ventral aspect of the medulla. The basic clinical features of lesions associated with cranial nerves are presented in Table 3.3. Remember: An easier simplified way of remembering the site of entering or exiting of CN from brainstem is 2, 4 and 4, i.e. apart from first two cranial nerves, CN III and IV from midbrain with V–VIII from pons and IX–XII from medulla.

Cerebellum Cerebellum consists of the midline vermis, two cerebellar hemispheres and a flocculonodular lobe. Primary role of the cerebellum concerns the planning and fine-tuning of the movements. The cerebellum exercises its influence on the contralateral upper motor neurones in the cerebral cortex and brainstem. The vermis specifically has a role in trunk muscle control with lesions resulting in truncal ataxia. Remember cerebellar lesions result in ipsilateral deficit.

Vascular anatomy (cranial) Figure 2.2 demonstrates the Circle of Willis at the base of the brain. CNS arterial supply is provided by a pair of internal carotid arteries (dividing into terminal branches of middle and anterior cerebral arteries) and a pair of vertebral arteries (uniting to form midline basilar artery at the junction between pons and medulla) forming the Circle of Willis. In terms of cerebral hemisphere, the blood supply is grossly as follows: anterior cerebral artery predominantly supplies the medial surface of the frontal and parietal lobes, including the motor

Anterior communicating artery Anterior cerebral artery

Middle cerebral artery Internal carotid artery

Posterior communicating artery Posterior cerebral artery Superior cerebellar artery

Basilar artery

Anterior inferior cerebral artery Vertebral artery Anterior spinal artery Posterior inferior cerebral artery Figure 2.2 Circle of Willis at the base of brain.

6

THE BASICS

Lateral corticospinal tract (skilled movement: same side of body)

Intermediolateral grey nucleus (sympathetic: T1 to L2 only)

Dorsal column (fine-touch/joint position/ vibration: same side of body) Central canal

Lateral spinothalamic tract (pain and temperature: opposite side of body)

Figure 2.3 Cross section of spinal cord.

and sensory cortices for the contralateral lower limb; middle cerebral artery with the largest cortical territory supplies almost the whole of the lateral surface of frontal, parietal and temporal lobes, including the speech areas in the dominant lobe, primary motor and sensory cortices for the contralateral whole body excluding the lower limb; posterior cerebral artery (derived from basilar artery) supplies the inferomedial temporal lobe and the occipital lobe, including the visual cortex. The vertebrobasilar system as a whole supplies brainstem, cerebellum and occipital lobe. With respect to internal capsule, the blood supply is derived from anterior choroidal artery arising from internal carotid artery, lateral striate branch of middle cerebral artery and recurrent artery of Heubner arising from anterior cerebral artery. The blood supply of basal ganglia is also derived from these arteries.

Spinal cord The vascular supply of the spinal cord is derived from radicular arteries arriving from the aorta. Artery of Adamkiewicz is the main arterial supply for the spinal cord from T8 to conus. Midthoracic region being a watershed zone is susceptible to vascular injury leading to ischemia or infarct. Figure 2.3 demonstrates a cross section from the spinal cord, including the intermediolateral column, representing sympathetic outflow and present from T1–L2. It is worth reviewing briefly the anatomy of the three tracts as outlined below from a basic Neuroanatomy text. The basic clinical information regarding these three tracts is as below:  Lateral corticospinal tract: Skilled movement (serving ipsilateral side).  Lateral spinothalamic tract: Pain and temperature sensation (serving contralateral side).  Dorsal column: Fine touch, joint position and vibration sense (serving ipsilateral side).

Peripheral nervous system Important muscle groups with their spinal roots, named nerve supply and actions to test, are summarised in Table 3.5. Similarly, a dermatomal map demonstrating the dermatomes needing examination during a routine neurological exam is included in Chapter 3.

NEUROLOGICAL HISTORY, EXAMINATION, SIGNS

3

7

Neurological history, examination, signs and localisation

This chapter is not intended to be exhaustive but rather is a brief summary of taking a neurological/neurosurgical history and performing a neurological examination. Here, we provide an overview of the process and a framework which allows a neurological diagnosis to be reached. One classical way of coming to a list of potential differential diagnoses when faced with a neurological/neurosurgical patient is to adopt the so-called where, what and why approach.

‘Where’ It is often the case that the neurologist or neurosurgeon, when confronted with a patient, will first ask themselves, where is the lesion?, meaning where is the predominant focus of pathology within the neurological system. The lesion may be at a single focus within the nervous system, such as entrapment of the median nerve at the wrist in the case of carpal tunnel syndrome or entrapment of an L5 nerve root in a patient with foot drop. Alternatively, the lesion may be multifocal, as in multiple sclerosis (MS) where demyelinating plaques may be found throughout the brain and spinal cord, or it may be diffuse or generalised, as in the case of encephalopathic patient with a reduced level of consciousness secondary to a systemic infection or metabolic derangement. In some instances, gross localisation is very straightforward, for example, in a patient with traumatic brain injury post a road traffic accident, it is relatively implicit to focus localisation within the brain. In case of a patient complaining of weak legs (see Chapter 9), the problem could however variably be within the brain, brainstem, spinal cord (central nervous system (CNS)) or within the anterior horn cell, nerve root, lumbar sacral plexus, peripheral nerves or neuromuscular junction (peripheral nervous system (PNS)) or be isolated to skeletal muscle. In the latter scenario, the neurological examination is pivotal to localising the problem where, for example, upper motor neurone (UMN) signs will point to a problem in the central nervous system and lower motor neurone (LMN) signs will point to a problem in the peripheral nervous system. The distribution of signs will also point towards the potential site of the lesion; therefore, hemisphere lesions usually lead to contralateral weakness affecting face, arms and legs, variably depending on the exact site of the lesion, whereas a cord lesion usually produces bilateral weakness with possible evidence of LMN signs at the level of the lesion and UMN signs below the level of the lesion with a sensory level. Patients may present with typical syndromes (Table 3.1) observed with pathology in different parts of the CNS, thereby further helping in localisation (also refer to Chapter 35).

‘What’ Having decided where the lesion lies, the next question to consider is what is the problem? Here we are thinking particularly of the aetiological group to which the potential diagnosis belongs. This is typically based upon the temporal sequence of events largely elicited by obtaining the history of the presenting complaint (Table 3.2).

‘Why’ Having decided where the potential lesion lies and also to which causative group the diagnosis may belong, the next step is to consider why might this disease or entity have occurred?. For example, the patient presenting with acute onset of right arm weakness and language disturbance is likely to have an abnormality localising to the left frontal lobe with the sudden onset suggesting a vascular cause. The question then arises regarding the reason for the occurrence of the vascular event. With a preceding history of trauma, an extradural haemorrhage may be the explanation, whereas a past history of smoking, diabetes and hypertension might point more towards an ischaemic stroke. This gathering of

8

THE BASICS

Table 3.1 Key areas within CNS with description of clinical syndromes related to pathology Relevant areas within CNS

Clinical syndromes related to pathology

Frontal lobe

Dominant frontal lobe only (Broca’s area): Broca’s or motor or expressive or non-fluent dysphasia with intact comprehension of written and spoken language but reduced verbal output with difficulty in putting words together and difficulty with repetition Primary motor cortex: Contralateral hemiparesis or hemiplegia Premotor (anterior to primary motor cortex) and supplementary motor cortex: Apraxia (i.e. performance of movements is impaired despite normal strength) as this area plays a role in contralateral motor programming Prefrontal area: Frontal lobe syndrome (problems with behaviour and cognition; intelligence and memory; apathy, including lack of motivation and abulia, i.e. lack of initiative or awareness) usually resulting from a large unilateral or bilateral lesions

Parietal lobe

Primary somatosensory cortex: Problem with perceiving somatic sensation on contralateral side of body Superior parietal lobule (usually with dominant hemisphere lesions): Usually result in ideomotor apraxia (inability to carry out tasks on command despite absence of motor deficit or weakness) or constructional apraxia (inability to copy a diagram) or astereognosia (inability to recognise an object without looking at it, for example a coin in the palm of a patient with eyes closed) Inferior parietal lobule (angular and supramarginal gyrus) in right hemisphere: Contralateral neglect (asomatognosia) despite intact somatic sensation, i.e. patients neglect the left side of body including dressing or looking after it; classically these patients when asked to draw a clock face only draw numbers on the right side. With left parietal lobe lesion, contralateral neglect is uncommon Inferior parietal lobule in left or dominant hemisphere: Gerstmann’s syndrome (finger agnosia, i.e. inability to recognise finger by name; agraphia without alexia, i.e. cannot write but can read; left–right disorientation and acalculia, i.e. inability to perform simple arithmetic calculations); with angular gyrus lesions (alexia, i.e. inability to read or comprehend written text and agraphia, i.e. inability to write); supramarginal gyrus and posterior part of superior temporal gyrus in dominant lobe (Wernicke’s or fluent or sensory or receptive aphasia characterised by fluent speech without meaning)

Occipital lobe

Contralateral homonymous haemianopia with macular sparing results with lesions of primary visual cortex, usually due to occlusion of a branch of posterior cerebral artery (for field defects associated with other sites, see Chapter 7)

Cerebellum

Unilateral cerebellar hemisphere lesions: Ipsilateral gait ataxia (impaired heel to toe test and broad-based gait), problem with coordination (intention tremor on finger to nose, i.e. increase in tremor amplitude as target is approached; dysdiadochokinesia on repeated movements and impaired heel to shin test) Cerebellar vermis: Truncal ataxia

Refer to Chapter 2 and Figure 2.1 therein.

NEUROLOGICAL HISTORY, EXAMINATION, SIGNS

9

Table 3.2 Potential causative groupings along with brief temporal and other clues associated with a particular aetiological group Aetiology

Characteristics/clues

Traumatic

Preceding history of trauma. Symptoms are typically acute but may, as in the case of chronic subdural haematoma, evolve over time

Vascular

Typically indicated by abrupt nature of onset, reaching maximum severity from outset

Infective

Typically a history evolving over days to weeks, although may evolve over months or be chronic. Supported by systemic markers of infection like raised white cell count or CRP/ESR

Metabolic

Typically symptoms evolve over days to weeks, although may be episodic or chronic

Malignant

Often symptoms evolve over weeks to months and may be due to direct tumour effects or as a paraneoplastic phenomena

Degenerative

Typically degenerative diseases evolve over months to years

Genetic

May be suggested by family history and typically symptoms evolve over months to years

Iatrogenic

This may be acute, subacute or chronic but clues are from the past medical history and history of medication exposure

Idiopathic

A causative category ascribed by a process of exclusion

Psychogenic

Be wary of ascribing a psychogenic cause, although very important to identify if this is the explanation

information regarding such associated factors should be covered in the history of the presenting complaint and other components such as the past medical history, the medication list, family history and social history.

The neurological history Many of the questions pertinent to be asked when considering patient complaining of specific neurological symptoms are covered in Parts II and III of this book dealing with presenting complaints and specific disease entities, which may be referred to when confronted with specific neurological complaints. Below are some additional points that should be included in the medical student or junior doctor clerking when obtaining a neurological history. In addition to detailing the patient’s name, age, occupation and marital status, in a neurological history it is also common to record patient’s handedness. Handedness suggests the dominant (language functioning) hemisphere of the brain, where nearly all right-handed people are left hemisphere dominant whereas only approximately 70% of left-handed people are left hemisphere dominant. Further understanding of patient’s handedness will increase understanding of impairment the patient may be experiencing due to their deficit. For example, a patient with right body predominant Parkinson’s disease who is right-handed will typically have greater impairment in fine finger function than a patient with left body predominant Parkinson’s disease who is right-handed.

Complaint and history of the presenting complaint (see Part II) Complaints may concern problems with senses, including sight, smell, hearing and taste. Other complaints may include blackouts, dizziness, headache, numbness, paraesthesia

10

THE BASICS

(pins and needles) and weakness in arms or legs. These are covered in detail in Part II. Disturbances with cognition, speech, swallowing and bowel or bladder function may also be reported. Psychiatric symptoms may also be present. A full history of presenting complaint is warranted, including mode of onset, provoking or triggering causes and progression of symptoms, for example gradual (with a slowly growing tumour) or rapid (e.g. in a vascular event like stroke). Also record the associated factors, for example in the case of a migraine headache, the associated factors of photophobia and nausea.

Past medical history Events from the past medical history are often useful in understanding why patients may have developed a particular disease. Check regarding meningitis, foreign travel and previous history of CNS trauma (minor or major, for example with reference to extradural or subdural haematoma). Past medical history may also help localise the lesion and point to the causative aetiology, for example the patient with a recent history of tooth abscess and dental extraction in preceding weeks who then develops focal onset of seizures affecting the right hand may have a brain abscess affecting the left motor strip. Medication history Neurological symptoms as a side effect of medication are extremely common. A detailed list of the medications (including anticonvulsants, antidepressants or antipsychotics), the dose and frequency of administration, as well as documentation of previous medication exposures is extremely important, for example a patient presenting with numbness of both feet evolving over months who has had chemotherapy in the preceding year may have a peripheral sensory axonal neuropathy secondary to chemotherapy. Isoniazid similarly can also cause peripheral neuropathy. Compliance with medications and any relevant side effects should be checked, for example this can be particularly important in patients with epilepsy as ongoing epileptic seizures may be due to non-compliance or due to taking anticonvulsant medication at an inadequate dose. Family history Conditions with a genetic basis are relatively common in neurological practice (see Part III). It is therefore important to obtain a detailed family history. Furthermore, understanding the patient’s fears about their symptoms or illness relies upon understanding of their prior exposure to and experiences of particular illnesses in their family. Social history Obtain history regarding smoking and drinking habits. This is relevant, for example peripheral neuropathy can occur in a patient with excessive alcohol drinking. Also detail exposure to illicit drugs and recent foreign or local travel. This may be relevant, for example in a patient with a lower motor neurone facial palsy who in preceding weeks suffered a tick bite while walking in a forest and now has neurological Lyme disease (neuroborreliosis). Functional history Understanding the level of disability or handicap a patient experiences due to an impairment (e.g. of arm function) is important in patients with long-term neurological conditions. One can work through a list of activities of daily living. Alternatively, one can work from head to toe asking the patient about specific functions, i.e. visual impairment, speech and swallowing impairment, upper limb impairment, impairment of bladder, bowel and sexual function and lower limb impairments, understanding along the way the consequences of these upon patient’s occupation or on performance of activities of daily living and the impact on family/carers. Systems review Always review other body systems by means of direct questioning at the end of the history to pick up additional associated features of a systemic disturbance which may highlight the cause of a specific neurological symptom. As an example, a patient with nocturnal

NEUROLOGICAL HISTORY, EXAMINATION, SIGNS

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breathlessness on lying flat may have neuromuscular and ventilatory impairment, which when considered with a history of weight loss, wasting and lack of sensory disturbance will point towards motor neurone disease.

Neurological examination The typical clerking style of neurological examination performed by medical students and junior doctors includes the neurological examination of the head and neck (cranial nerve (CN) examination) as well as the upper and lower limbs. Additional routines of examination are also used to specifically test the cerebellar system, gait (see Chapter 11) and extrapyramidal system, domains of cognition or lobar functions of the brain (Table 3.1).

Suggested order of examination General examination as a screening test including general inspection; mental status examination (not fully and formally undertaken on every neurological patient, however, may be important as neurological and psychiatric symptoms may coexist in illnesses like dementia), including checking patient’s appearance, behaviour, mood and for presence of delusions or hallucinations among others; higher mental function and speech; cranial nerves; upper and then lower limbs (inspection, tone and power); reflexes; sensory exam and finally coordination and gait. Higher mental function and speech Check patient’s conscious level (using Glasgow Coma Scale as detailed in Appendix 2); orientation in time, place and person and finally perform a cognitive screening using abbreviated mental test score or mini-mental state examination if there is suspicion of cognitive impairment. Higher mental function may be impaired in various lobar syndromes, as detailed in Table 3.1. Note that ‘apraxia’ refers to the inability to perform an action despite an intact motor and sensory function while ‘agnosia’ refers to impaired perception despite the presence of an intact sensory function during neurological examination. Check speech (usually assessed during obtaining history) for dysphasia syndromes (Table 3.1), including conduction dysphasia seen with lesions of the arcuate fasciculus (fibre tract connecting Broca’s and Wernicke’s area) and characterised mainly by impaired repetition; dysarthria implying difficulty with articulation by asking the patient to say, for example, ‘British Constitution’ (types include cerebellar characterised by slurred (drunk) and scanning speech, spastic as seen in pseudo-bulbar palsy in motor neurone disease and characterised by ‘Donald Duck’-type voice, monotonous speech in extrapyramidal disease and bulbar speech in lower motor neurone syndromes like facial nerve palsy and characterised by nasal quality to speech) and dysphonia (impaired speech volume due to problem with respiratory muscles, for example myasthenia gravis). Cranial nerves For a detailed paper on the topic of ‘cranial nerve examination’, refer to Asghar and Abhinav 2011. Brief notes on examination of CN are as follows (Table 3.3):
I (Olfactory): Smell is not routinely tested unless patients complain of problem with smell; if needed, check ability of each nostril to distinguish different types of smell, including camphor, peppermint and others.
II (Optic): Each eye should be checked separately. Check acuity (Snellen chart), visual fields (to confrontation) and pupils (size, shape, reactivity to light, including direct and consensual response and accommodation) and perform a detailed opthalmoscopic examination inspecting the optic disc for papilloedema or atrophy.
III (Oculomotor), IV (trochlear), and VI (abducens): Check extraocular movements for full range of motion and evidence of diplopia, nystagmus, ptosis or internuclear opthalmoplegia (INO) (Chapter 18). Nystagmus refers to involuntary eye oscillations and can be normal at extreme lateral gaze. Direction of the fast phase should be noted; nystagmus can occur in the context of cerebellar or vestibular lesions. INO, for example, due to multiple sclerosis results due to a lesion in the medial longitudinal fasciculus and refers to failure of adduction of the ipsilateral eye with nystagmus in contralateral eye on abduction.

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THE BASICS

Table 3.3 Summary of signs and symptoms in cranial nerve lesions with their associated aetiology Cranial nerve

Signs or symptoms of a lesion

Cause or lesion

I (Olfactory)

Change in sense of smell

Nasal obstruction Polyps or foreign bodies Viral infections

Unable to identify common substances

Neurological causes Head injury Nasofrontal tumours Parkinson’s disease Alzheimer’s disease

II (Optic) (see Chapter 7)

Monocular blindness

Lesions of the eye Cataracts Intraocular haemorrhage Retinal detachments Diseases of the optic nerve Multiple sclerosis Tumours

Bitemporal haemianopia

Compression of optic chiasm Pituitary tumour

Homonymous haemianopia

Lesions of the optic tract Vascular lesions Neoplasm Optic radiation Lesions of the occipital lobe

Visual inattention

Parietal lobe lesions

Reduced visual fields

Glaucoma Chronic papilloedema

NEUROLOGICAL HISTORY, EXAMINATION, SIGNS

13

Marcus Gunn Pupil (relative afferent pupillary defect) observed during the swinging flashlight test [patient’s pupils constrict less (therefore appearing to dilate) when the light swings from the pupil of the unaffected eye to the pupil of the affected eye]

Damaged optic nerve pathway—indicating a decreased pupillary response to light in the affected eye (this detects less light than the functioning pathway)

Constricted pupil

Horner’s syndrome Opiate overdose Brainstem stroke

Nystagmus

Physiological Congenital Visual impairment (difficulty in fixing gaze) Vestibular disease Cerebellar disease

Papilloedema

Increased intracranial pressure Tumour Abscess Encephalitis

III (Oculomotor)

Divergent squint and diplopia (eyes down and out)

Paralysis of extraocular muscles (superior rectus, inferior rectus and medial rectus)

Ptosis

Paralysis of levator palpebrae Horner’s syndrome Myasthenia gravis

Dilated pupil

Paralysis of sphincter pupillae Tumour Aneurysm Brainstem stroke

(continued )

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THE BASICS

Table 3.3 (Continued) Cranial nerve

Signs or symptoms of a lesion

Cause or lesion

IV (Trochlear)

Eye elevation and outward rotation and diplopia (on looking down)

Paralysis of superior oblique muscle Tumour Aneurysm

V (Trigeminal)

Localised pain and vesicular eruption

Herpes zoster infection

Anaesthesia and dissociated sensory loss

Syringobulbia

Brisk jaw jerk

Bilateral upper motor neuron lesion

Loss of corneal reflex, paralysed muscles of mastication (deviation of jaw towards side of the lesion with unilateral lesion) and loss of facial sensation

CN V palsy

Neoplasm Infection VI (Abducens)

Convergent squint and horizontal diplopia (with all movements excluding adduction)

Paralysis of lateral rectus muscle Tumour Aneurysm

VII (Facial)

Unilateral complete facial paralysis, hyperacusis, altered taste and impaired corneal reflex on affected side

Bell’s palsy

Unilateral lower facial palsy only (as forehead or frontalis has bilateral UMN innervations, so relative sparing of forehead is observed with unilateral UMN lesion)

UMN lesion

Stroke Tumour MS Unilateral entire facial palsy (observed with LMN lesion where complete ipsilateral palsy with droopy mouth and loss of eyebrow lines and nasolabial folds is noted)

LMN lesion

NEUROLOGICAL HISTORY, EXAMINATION, SIGNS

15

Stroke and tumour (acoustic neuroma) Ramsay Hunt syndrome Lyme disease, TB and HIV Diabetes and sarcoidosis VIII (Auditory)

Conductive deafness

Ear disease Otitis externa or otitis media Paget’s disease Perforated ear drum

Sensorineural deafness

Congenital Acquired Presbycusis (ageing) Noise induced Ototoxicity (drugs)

IX (Glossopharyngeal)

Attacks of dizziness and deafness

Acoustic neuroma (benign tumour). As it expands, it may compress adjacent CN V–VII

Altered sensation to palate and pharynx

CN IX palsy Base of skull tumour Stroke or trauma

X (Vagus)

Weak cough or dysphonia

Lesion of the recurrent laryngeal branch

Asymmetrical soft palate (with unilateral weakness palatal deviation towards the normal side) and loss of gag reflex

CN X palsy

Base of skull tumour Stroke or trauma XI (Accessory)

Loss of power to sternocleidomastoid (SCM) or trapezius muscles

CN XI palsy

(continued )

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THE BASICS

Table 3.3 (Continued) Cranial nerve

Signs or symptoms of a lesion

Cause or lesion Tumour Stroke Trauma

XII (Hypoglossal)

Tongue deviation (towards side of lesion) or weakness

Lower motor neuron lesion

Tongue fasciculation

Motor neurone disease

Adapted from Asghar and Abhinav (2011).















V (Trigeminal): Check facial sensation (pinprick and light touch) in all three divisions (ophthalmic—V1, maxillary—V2 and mandibular—V3), corneal reflex (CN V1—afferent and CN VII—efferent) and motor function (CN V3) by asking patient to open their mouth and clench in order to feel masseter and temporalis (muscles of mastication). VII (Facial): Ask patient to raise eyebrows or look at the ceiling, puff up their cheeks or whistle and screw their eyes shut. Taste can also be checked in the anterior two-thirds of the tongue. Distinction between UMN type versus LMN type of facial nerve weaknesses is important (Table 3.3). Bell’s palsy with its clinical features (as listed in Table 3.3) is a diagnosis of exclusion and typically has an abrupt onset with features of a unilateral LMN facial nerve palsy. Bell’s phenomenon (inability to close eyes with rolling up of eye on attempted closure) may be seen. Short course of steroids (Prednisolone) may be tried with artificial tears and eye patch to protect the cornea. VIII (Vestibulocochlear): Whisper a number while blocking the contralateral ear and ask patient to repeat the number. If there is unilateral hearing disturbance, carry out Weber’s and Rinne’s tests to distinguish between conductive and sensorineural hearing loss. IX (Glossopharyngeal) and X (vagus): Ask patient to say ‘Ahh’ and look at the uvula for central elevation. Gag reflex (CN IX—afferent and CN X—efferent) may be checked. XI (Accessory): Ask patient to shrug their shoulders (trapezius) or turn head to one side against resistance (sternocleidomastoid). XII (Hypoglossal): Check for fasciculation and wasting with tongue inside mouth (LMN lesion). Ask the patient to move it from side to side checking for any slowing of the tongue movement (UMN lesion).

Upper and lower limbs Typically start with inspection and then examine tone and power. Tendon reflexes, sensation and finally coordination and gait are also tested. Specifically inspect for muscle wasting or atrophy (in LMN syndromes) and fasciculations (e.g. in motor neurone disease) and observe the posture (e.g. stooped posture of Parkinson’s) and check for presence of any abnormal movements, for example tremor (see Chapter 20). Check for pyramidal drift (pronation and drifting down of outstretched arms) occurring for example with UMN lesions in corticospinal tract. Tone Testing tone can help determine whether the lesion is within the central or peripheral nervous system. Tone may be increased, decreased (hypotonia) or normal and is best assessed at wrist, elbow, hip and knee. If increased, it can be either in spastic or rigid fashion. Lesions

NEUROLOGICAL HISTORY, EXAMINATION, SIGNS

17

Table 3.4 Muscle strength grading (MRC scale) Grade

Muscle strength

0

No contraction

1

Flicker of contraction

2

Movement with elimination of gravity

3

Active movement against gravity

4

Active movement against resistance (4 slight, 4 moderate and 4þ strong)

5

Normal power

affecting the corticospinal tract (UMN) produce a spastic increase in tone, best elicited by a rapid flexion extension movement of the elbow where a so-called spastic catch or a sudden increase in tone may be felt. In contrast, a rigid increase (increased through a whole range of movement) in tone typically localises to problems within the basal ganglia (extrapyramidal system, for example Parkinson’s disease) and is best elicited either by a slow flexion extension movement at the elbow, knees or ankles or by a slow circling movement at the wrist. Rigidity may be described as ‘lead pipe’ and when combined with breaks or tremors as being ‘cogwheeling’. Rigidity may be heightened by asking the patient to perform movement of the contralateral limb (synkinesis). Power testing Power testing involves assessing power in a given muscle group around each joint. For example at the elbow, power is assessed for elbow flexion and extension. Power testing is documented using the Medical Research Council (MRC) grading scale shown in Table 3.4. Always compare with the strength on the contralateral side. It is important to be aware of the muscle groups being tested along with innervating nerve roots and named nerves (Table 3.5). Reflexes Reflex (segmental levels in Table 3.5) testing requires practice and reflexes may be absent, decreased, normal, increased and finally increased with clonus (contraction of muscle when stretched and tested for at the ankle and quantified in terms of number of beats). Increased reflexes are associated with a lesion in the UMN pathway (corticospinal tract) whereas decreased or absent reflexes occur with a problem in the peripheral nervous system (LMN pathway) with a loss of a reflex or reflexes being due to failure of either the afferent (sensory) or the efferent (motor) arm of the reflex arc. The plantar response is assessed using stimulus on lateral sole with an upgoing or extensor plantar or Babinski sign (associated with UMN lesions within the corticospinal tract) being defined as extension of big toe with fanning out or spreading out of other toes. Normal response is flexion of the toes. Note on UMN versus LMN lesions
LMN lesions lead to hypotonia, hyporeflexia or areflexia; fasciculations with atrophy of the affected muscles therefore causing a flaccid paralysis on the same side and at the level of the lesion.
UMN lesions lead to hypertonicity, hyperreflexia with or without clonus, Babinski sign, loss of abdominal and cremasteric reflex and disuse atrophy. UMN lesions always lead to spastic weakness which is below the level of the lesion and could be ipsilateral (if lesion affects corticospinal tract in spinal cord) or contralateral (if lesion is between the cerebral cortex and medulla above the pyramidal decussation).

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THE BASICS

Table 3.5 Important muscle groups and spinal nerve roots with reflexes for upper and lower limbs Segment

Muscle

Action

Nerve

C5, C6

Deltoid

Abduct arm

Axillary

C5, C6

Biceps

Elbow flexion

Musculocutaneous

Biceps

C5, C6

Brachioradialis

Forearm flexion with thumb up

Radial

Supinator

C6, C7, C8

Triceps

Elbow extension

Radial

Triceps

C6, C7

Extensor carpi radialis

Wrist extension

Radial

C7, C8

Extensor digitorum

Finger extension

Posterior interosseous (branch of radial nerve)

C7, C8, T1

Flexor digitorum profundus (ulnar part)

Flexion of distal phalanx of fingers (4 and 5)

Ulnar

C7, C8, T1

Flexor digitorum profundus (radial part)

Flexion of distal phalanx of fingers (2 and 3)

Anterior interosseous (branch of median nerve)

C8, T1

Interossei

Abduct fingers

Ulnar

C8, T1

Abductor pollicis brevis

Thumb abduction

Median

C8, T1

Opponens pollicis

Thumb opposition

Median

L1, L2

Iliopsoas

Hip flexion

Lumbosacral plexus

L5, S1

Gluteus maximus

Hip extension

Inferior gluteal

L3, L4

Quadriceps

Knee extension

Femoral

L5, S1

Hamstrings

Knee flexion

Sciatic

L4, L5

Tibialis anterior

Ankle dorsiflexion

Deep peroneal (branch of common peroneal nerve)

L5, S1

Extensor hallucis longus

Great toe extension

Deep peroneal

S1, S2

Gastrocnemius

Ankle plantarflexion

Tibial (branch of sciatic)

L5, S1

Peroneus longus and brevis

Foot eversion

Superficial peroneal (branch of common peroneal nerve)

L5, S1

Posterior tibialis

Foot inversion

Tibial

Major innervations indicated in bold.

Reflex

Knee

Ankle

NEUROLOGICAL HISTORY, EXAMINATION, SIGNS

19

Sensory Different modalities of sensation are conveyed by different pathways (see Figure 2.3) and each should be assessed. Always teach the test first prior to carrying it out. Dorsal column (fine touch, joint position and vibration sense on ipsilateral side) Vibration sense is assessed with 128 Hz tuning fork; start with sternum to familiarise patient with the vibration sense and then apply to bony prominences (including base of big toe, medial malleolus, knee and elbow) starting distally. If sensation is normal distally, there is no need to carry out tests more proximally. Test for joint position sense is taught with patient’s eyes open followed by movement of the joint with patient’s eyes closed and asking them regarding the direction of movement of the joint, i.e. up or down. Light touch is tested using cotton wool or fingertip in all dermatomes (Figure 3.1), including those in the affected ones.

C2 C2

C3 C3 C4 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12

C5

T2 T1 C6

L1 C6

S3 S4

C7 C8

C4 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11 T12 L1 L2

C3 C4 T2 C5 T2

C6 T1

S4 S5

C6

S3 C8 C7

L2

L2 S2 L3 L3 L4

L5

L5 S1

L4 S1

S1 L5

L5

Figure 3.1 Dermatomes represented on anterior and posterior aspects of the body.

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THE BASICS

Spinothalamic tract (pain and temperature sensation on contralateral side) Pain (tested using pinprick) sensation is tested in all dermatomes (Figure 3.1) including those in the affected ones with patient’s eyes closed. Teach the patient first by applying the pin in a normal area of skin. Temperature sensation is not tested routinely; however, it can be carried out using test tubes with hot and cold water. With sensory losses (see Chapter 10), always map out the area and distribution, for example glove and stocking distribution with diabetic peripheral neuropathy (see Chapter 24).

Gait and coordination Gait assessment with associated disturbances is covered in detail in Chapter 11. In brief, ask patient to walk normally followed by heel to toe test (indicates ataxia if patient is unable to perform the test). Romberg’s test (patient stands with their feet together followed by eyes closed) is positive if patients lose their balance with eyes closed and indicates posterior column pathology (joint position dysfunction leading to sensory ataxia). If unable to do this with eyes open, cerebellar ataxia may be implied (however, not Romberg’s positive). Note that Romberg’s test is useful for distinguishing between cerebellar and sensory ataxia in a patient with a broad-based gait. Coordination is typically tested with finger to nose test; heel–shin testing and using repeated movements (rapid pronation and supination of hand on dorsum of other hand; impairment with this is referred to as dysdiadochokinesis and occurs with cerebellar pathology).

Reference Asghar R, Abhinav K (2011) Cranial nerve examination. International Journal of Clinical Skills 5 (1): 56–63.

NEUROLOGICAL INVESTIGATIONS

4

21

Neurological investigations

Neurophysiology Electroencephalogram (EEG)
Used for recording the electrical activity of the brain via electrodes attached to the scalp.
Principal use of EEG is in the diagnosis and management of different seizure disorders with the EEG being performed during ictal and interictal phases.
Can be recorded with video monitoring.
Diagnostic yield can be increased with the use of forced hyperventilation (e.g. triggering spike and wave activity), photic stimulation, sleep deprivation and repeating the EEG.
While interpreting interictal EEG, background rhythm and paroxysmal changes need to be considered. Normal background rhythm is called ‘alpha’ at 8–13 Hz (mainly in the occipital lobes when one is awake and quiet). Slowing of the background rhythm can occur in metabolic encephalopathy (renal and hepatic failure), drug overdose and other degenerative conditions.
Paroxysmal changes (spikes 48 h–14 days). CSF is characteristically dark. Majority of pathology is hypointense.
T2 weighted image (T2WI): The sequence of choice for highlighting pathology which is usually hyperintense including cerebral oedema. CSF is characteristically bright while

24

THE BASICS

Figure 4.1 T1WI axial image of the brain (note CSF is dark).

bone and fat are dark (Figure 4.2). Acute (1–3 days) and early subacute (>3 to 7 days) blood is hypointense while blood (7–14 days) is hyperintense. Remember: CSF signal intensity can be used to determine the type of sequence, i.e. hypointense in T1WI compared to hyperintense in T2WI. Bone is dark in both. Interpretation of blood on MRI scan is complex with varying signal intensities depending on the age of the clot and its breakdown product.




STIR sequences combine T1 and T2 suppressing signal from fat. Used in spinal pathology.
Diffusion-weighted imaging and perfusion-weighted imaging are used in patients with suspected ischaemic brain injury.
Magnetic resonance spectroscopy relies on spectroscopy of other molecules and atoms besides hydrogen, thereby providing information on chemistry of specific lesions like tumours or abscess. One use for example is in differentiating between the two aforementioned using choline and lactate peaks.
MRI can also be applied to delineate arterial (MR angiogram, for example used in screening for aneurysms, neck vessel dissection) or venous anatomy (MR venogram, for example used in suspected cases of venous sinus thrombosis).

NEUROLOGICAL INVESTIGATIONS

25

Figure 4.2 T2WI axial image of the brain (note CSF is bright).

Angiography
Catheter angiogram remains the gold standard for imaging intra- and extracranial vessels.
Local anaesthetic/sedation is used prior to the insertion of the catheter into the femoral artery and then into the carotid or vertebral artery origin with the help of an image intensifier. Computerised digital subtraction angiography technique is performed.
The main indications are for diagnosing cerebral aneurysms or arteriovenous malformations in cases of suspected subarachnoid haemorrhage. Interventional angiography involving coiling of the aneurysm is being increasingly used in the treatment of aneurysms (see Figure 16.2).
Risk of a resulting permanent neurological deficit is about 0.1%.

Lumbar puncture and CSF analysis


A widely used investigation in neurological and neurosurgical practice. Indications include suspected meningitis of bacterial, viral or fungal aetiology; CNS demyelinating conditions like MS and peripheral demyelinating neuropathy, for example GBS and in cases of suspected SAH with a normal CT scan.
In adults, intercristal line (line connecting the superior border of the iliac crests) passes through the spine at L4 spinous process or between L4 and L5 spinous processes. The recommendation is to use L4 and L5 interspace or a level higher (L3 and L4).

26

THE BASICS

Remember: Although the dural sac extends to S2, spinal cord terminates at the level of the vertebral bodies of L1 and L2; therefore, if correctly performed at an appropriate level, LP should not damage the spinal cord.

Place patient in a left lateral position, with the shoulders square and pillow under the head and between the knees. Ideally a 22G needle with stylet in situ (under a strict aseptic technique and following infiltration of a local anaesthetic) is inserted aiming slightly cranially (or towards the umbilicus).
The layers traversed through include skin, subcutaneous tissue, supra and then interspinous ligaments, ligamentum flavum, epidural space and then through the dura and arachnoid into the subarachnoid space. Removal of stylet will lead to a flow of CSF. Using a three-way tap, measure the opening pressure and collect samples in at least three tubes: microscopy, cell count, culture, sensitivity and gram stain; protein, glucose and oligoclonal bands (on electrophoresis); cytology for the presence of malignant cells (e.g. in carcinomatous meningitis). Closing pressure should be measured if the opening pressure was raised followed by reinsertion of stylet and withdrawal of the needle. A blood sample should be taken at the same time for blood glucose, protein and oligoclonal bands (e.g. if diagnosis of MS suspected) (Table 4.2).

Table 4.2 Different clinical conditions with their characteristic CSF findings Cells (mm3)

Protein (mg/dL)

Glucose

Comments

Clinical condition

Opening pressure (cm H2O)

Normal

7–18

50 years (average age of onset around 70 years) with F:M ¼ 2:1. Aetiology is unknown. Clinical symptoms include headache (commonest symptom), jaw claudication (pain on chewing) and visual disturbance, including amaurosis fugax and blindness, which is usually irreversible. Patients may also experience systemic symptoms, including fever and malaise, and may further have musculoskeletal symptoms ranging from aching and stiffness to weakness affecting proximal muscles like shoulders and hips (polymyalgia rheumatica). Examination in GCA may yield tenderness of temporal arteries (scalp tenderness) on palpation (alternatively patients may complain of pain on combing hair). ESR is usually elevated (>40 mm/h). Temporal artery biopsy is highly specific for the diagnosis. Treatment using high-dose steroids (e.g. prednisolone) eventually tapered gradually is aimed at relieving symptoms and preventing the irreversible complication of blindness.

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CONDITIONS: APPLYING THE BASICS

Remember: Treatment with high-dose steroids in patients with a clinical suspicion of GCA should not be delayed in order to obtain a definitive diagnosis using temporal artery biopsy due to risk of blindness in this condition.

Idiopathic intracranial hypertension (IIH) A condition characterised by increased intracranial pressure in the absence of a mass lesion or hydrocephalus. Also known as pseudo-tumour cerebri or benign intracranial hypertension (Remember the condition is anything but benign!). It tends to affect obese women with a peak incidence in third decade. Associations include obesity, hypervitaminosis A, oral contraceptive use and others. Although by definition the condition is idiopathic, it may be secondary to venous sinus thrombosis. Symptoms classically include headache and visual disturbance, including transient blacking out of vision, constricted visual fields, poor colour vision and reduced visual acuity. Predominantly visual signs on examination are elicited and include papilloedema (extremely common), enlargement of blind spot with constricted visual fields and poor colour vision, reduced visual acuity and CN VI palsy (a false localising sign). CT or MRI with and without contrast is aimed at excluding both an intracranial mass lesion and a venous sinus thrombosis (using MR venography). Small slit-like ventricles may be seen. Lumbar puncture opening pressure in IIH patients is >20 cm H2O with an otherwise normal cerebrospinal fluid analysis. All patients with suspected IIH should have a comprehensive opthalmological testing, including visual acuity, field testing (with perimetry), slit lamp examination and fundal photographs. Remember: Spontaneous resolution may occur; however, these patients are at risk of permanent visual loss, so they require long-term follow-up and regular opthalmological evaluation.

Treatment options include weight loss and use of diuretics like Acetazolamide (carbonic anhydrase inhibitor). If these fail, surgical options include optic nerve sheath fenestration (for those with visual loss without headache) or shunts (lumbo- or ventriculoperitoneal for patients with headache as the predominant feature of the disease).

Trigeminal neuralgia (TN) TN is one of the craniofacial pain syndromes characterised by severe paroxysmal electric shock like pain, usually triggered by sensory stimuli including touching, shaving or eating and lasting a few seconds in the distribution of one or more divisions of the trigeminal nerve (i.e. ophthalmic—V1, maxillary—V2, mandibular—V3). It can be unilateral or bilateral (association with multiple sclerosis (MS). TN can occur in the context of neurovascular compression of the trigeminal nerve at its root entry zone (REZ) usually by a loop of superior cerebellar artery and other structural abnormalities like a posterior fossa tumour or in the context of demyelination in the brainstem, for example in MS. History is as above and examination is usually normal unless TN is associated with a tumour or is related to MS. MRI (with neurovascular protocol) is used to examine REZ for evidence of neurovascular compression, to look for other structural abnormalities like tumours or to exclude demyelinating plaques, for example in MS. Treatment is usually medical with use of drugs like Carbamazepine or Gabapentin. Surgical options (reserved for medically resistant cases or for cases with significant intolerable side effects from medications) include among others microvascular decompression via a retrosigmoid craniotomy (involving displacement of offending vessel from the REZ of trigeminal nerve) or percutaneous trigeminal rhizotomy (using glycerol injection or radio frequency coagulation). Spontaneous remission of TN may occur and last weeks to months.

TRANSIENT ISCHAEMIC ATTACKS (TIAs)

13

55

Transient ischaemic attacks (TIAs)

‘An acute neurological event affecting cerebral or retinal function with symptoms lasting less than 24 hours.’ This 24 h cut-off is arbitrary, and about one-third of patients with TIA fulfilling these criteria have evidence of ischaemic damage on brain MRI scanning. Therefore, a new definition was proposed by the American Stroke Association Stroke Council: ‘A transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction.’

DEFINITION

EPIDEMIOLOGY
Incidence : " with age: Estimates vary widely


and TIAs are probably still underrecognised. The general incidence in the United Kingdom: Around 0.5 per 1000 in the population as a whole, rising to an estimated 6.4 per 1000 in people over 85 years (data from OXVASC population study, Oxford, UK, 2002–2004).

AETIOLOGY AND PREVENTION Aetiology similar to thromboembolic stroke (see Chapter 14) and due to an artery-to-artery emboli or cardiac emboli. Prevention includes management of risk factors, i.e. antihypertensives (not beta-blockers), good diabetic control, cholesterol-lowering agents, regular exercise, smoking cessation, limitation of alcohol intake (particularly binge drinking) and judicious use of HRT in high-risk patients. ASSOCIATIONS/RISK FACTORS
Principal risk factors: Atrial fibrillation

(AF), hypertension, current smoking, diabetes, hypercholesterolaemia and family history. Other vascular disease (ischaemic heart disease and peripheral vascular disease), prior TIA or stroke.
Other risk factors/associations: Excess alcohol (binge drinking), polycythaemia, drugs, for example combined OCP and HRT, race, obesity and physical inactivity, raised CRP and plasma homocysteine, and lower socio-economic status. CLINICAL FEATURES (HISTORY/EXAMINATION)

Clinicians, including stroke specialist neurologists, often disagree about perceived likelihood of a TIA diagnosis.
Clinical features making diagnosis of TIA: More likely include rapid onset (within seconds), history suggestive of typical vascular syndrome, especially carotid territory (see Chapter 14) and physical signs corresponding to symptoms and multiple risk factors for TIA.
Features decreasing likelihood for TIA: Previous unexplained neurological symptoms and non-specific symptoms such as dizziness without vertigo, syncope and cognitive impairment.
Amaurosis fugax: Type of TIA characterized by sudden loss of monocular vision, either complete (central retinal artery) or sectoral/central (branch retinal artery). The central retinal artery originates from the ophthalmic artery, a branch of the internal carotid artery. INVESTIGATIONS
Brain imaging: Useful

to differentiate between TIA and mimics and exclude intracranial haemorrhage (CT) and to identify patients with cerebral infarction (diffusion-weighted MRI).
Arterial imaging:  Carotid Doppler ultrasound: Detects narrowing using blood flow velocity and may identify plaque features reflecting risk. Limited by calcification and arterial anatomy.  CT angiography (CTA) and contrast MR angiography (MRA): More accurate than carotid Doppler ultrasound, and can evaluate intracranial arterial stenosis. Beware that contrast agents carry risks for patients with renal impairment.
Electrocardiography (ECG): Arrhythmias (particularly AF) and myocardial infarction (may indicate ventricular aneurysm)

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CONDITIONS: APPLYING THE BASICS




Echocardiography: Valvular heart disease, for example mitral valve disease (association with AF), enlarged left atrium (also associated with atrial fibrillation) and intracardiac thrombus. Use of a contrast agent (micro-bubbles) may show a patent foramen ovale.
Cardiac rhythm monitoring: Asymptomatic AF may be detected using cardiac rhythm monitoring, for example ward-based monitoring or 24 h tape. MANAGEMENT

Early assessment: The risk of stroke is highest very early after TIA; therefore, patients with suspected TIA require easy and rapid access to specialist review and investigation. For moderate and high-risk patients (e.g. ABCD2 score of 4 or above), this is typically within 24 h. For low-risk patients, it may be reasonable for review to occur within 7 days. Medical management (see Chapter 14): According to two studies (SOS-TIA and EXPRESS), medical management alone can reduce 30 day stroke risk by 80% following TIA. Patients with AF (including paroxysmal AF) have a significant risk of stroke after TIA of about 4–18% per annum, depending on the presence of other risk factors such as age, hypertension, congestive cardiac failure and diabetes. Remember the association between AF and the risk of TIA/stroke.




Antiplatelet agents: With proven benefit include Aspirin, dipyridamole (Modified release dipyridamole reduces risk of stroke following TIA, over and above only in combination with aspirin. Immediate release preparations appear to be ineffective) and clopidogrel.  Initial treatment: Aspirin 300 mg daily, aspirin 75 mg þ dipyridamole modified release 200 mg bd or clopidogrel 75 mg daily are reasonable. In high-risk patients, a combination of aspirin 75 mg and clopidogrel 75 mg daily, after loading with 300 mg of each drug, may be beneficial.  Subsequent treatment (e.g. after 14 days): A combination of aspirin and modified release dipyridamole is more effective than aspirin alone (ESPRIT and ESPS2 trials). Clopidogrel appears to be equivalent to aspirin and dipyridamole in combination (PROFESS trial).
Anticoagulants: Patients with AF should be started on anticoagulants after TIA as soon as haemorrhage is excluded by brain imaging (with CT). Warfarin is currently the most effective drug for prevention of stroke after TIA in AF (WARRS trial versus aspirin, ACTIVE-W trial versus aspirin/clopidogrel combination), but causes more haemorrhagic strokes. Aspirin 75–100 mg daily plus clopidogrel 75 mg daily prevents more strokes than aspirin alone, but causes more haemorrhages of all types (ACTIVE-A trial). Clopidogrel is not currently licensed in the United Kingdom for treatment of TIA, but in combination with aspirin this is a reasonable alternative to warfarin in patients unable to take warfarin, for example due to high risk of falls. Remember: Warfarin is the most effective drug for prevention of stroke after TIA in AF.

Dabigatran is a new anticoagulant, at least as effective as warfarin in preventing stroke in atrial fibrillation, with equal or lower haemorrhage rates (RELY study).
Antihypertensive agents: The strongest evidence for prevention of stroke (PROGRESS trial, Lancet 2001) is for a combination of a thiazide diuretic (specifically indapamide) and an ACE inhibitor (specifically perindopril). Beta-blockers appear to be relatively ineffective in preventing stroke.
Cholesterol-lowering agents: Statins significantly reduce the risk of stroke in patients with cerebrovascular disease and cholesterol levels of 3.6. Simvastatin 40 mg once daily is a suitable initial treatment.

TRANSIENT ISCHAEMIC ATTACKS (TIAs)

57

Surgical management: Carotid endarterectomy and stenting:
Endarterectomy reduces death and stroke in patients with carotid stenosis of 70% (loss of 70% of the lumen) on the side corresponding to symptoms.
Endarterectomy benefits patients with 50–69% stenosis if performed: On patients with low surgical risk and by surgeons with low complication rates.
Endarterectomy: Perform as soon as possible after the index event, provided the patient is stable (usually within 2 weeks). Lower rate of immediate complications (especially non-disabling stroke) than endovascular stenting and has greatest benefit over stenting in older patients. Stenting is equivalent to endarterectomy in young patients. Use aspirin both before and following endarterectomy to reduce embolic complications. Lifestyle modifications: Following TIA, these are important: smoking cessation, improved diabetic control (including medication, exercise and low glycaemic index diet), dietary changes (especially low saturated fat and low salt), increased exercise (5 or more days per week, 30 or more min duration each to slight breathlessness), weight loss in obese patients, alcohol reduction to recommended limits (3 units per day for men, 2 units for women per day in the United Kingdom) with avoidance of binge drinking and avoidance of the combined oral contraceptive and HRT. Although TIAs by definition completely resolve, they are often markers of significant risk.
About 15% of strokes are preceded by a TIA, and within a year of TIA up to a quarter of patients die.
About half of the patients going on to have a stroke within 30 days after TIA have their stroke within 24 h.
Factors associated with increased risk of stroke after TIA: Carotid stenosis, abnormality on diffusion-weighted MRI (early after TIA this may show ischaemic changes which approximate to areas of acute infarction), repeated TIA events over a short period (e.g. 1 month or less), increasing age, hypertension, clinical features—hemiparesis and speech disturbance, symptom duration and diabetes.
Patients must be advised to inform the Driver and Vehicle Licensing Agency (DVLA) of being advised to not to drive for 1 month following a TIA (due to risk of further TIA and stroke). If there are no symptoms after this time, patients may start driving again.
Individualising risk of stroke after TIA: The ABCD2 score (Table 13.1) is widely used to estimate individual risk of stroke after TIA and guide management. Patients are scored (total score range 0–7) and then categorised as low, medium or high risk. PROGNOSIS

Table 13.1 ABCD2 score to estimate individual risk of stroke after TIA Calculation of ABCD2 score Risk factor

Estimation of individual stroke risk

Add score

Total score

Risk stratum

% Risk of stroke within time 2 days

7 days

90 days

Age 60 years or more

1

0–3

Low

1.0

1.2

3.1

First BP  140/90

1

4–5

Moderate

4.1

5.9

9.8

6–7

High

8.1

11.7

17.8

Clinical features Speech disturbance

1 (continued )

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CONDITIONS: APPLYING THE BASICS

Table 13.1 (Continued) Calculation of ABCD2 score Risk factor

Estimation of individual stroke risk

Add score

Total score

Risk stratum

% Risk of stroke within time 2 days

Unilateral weakness

7 days

90 days

2

Duration 10–59 min

1

60 min or more

2

Diabetes

1

DIFFERENTIAL DIAGNOSES (TABLE 13.2)

Table 13.2 Differential diagnoses for TIA with points to note Clinical conditions

Points to note

Hypoglycaemia

Check blood glucose (usually capillary) immediately in all patients with suspected stroke or TIA

Migraine (Chapter 12)

Migraine aura resulting from temporary cerebral dysfunction can be mistaken for TIA. History and sequence of events important

Seizures (Chapter 17)

Todd’s paresis following a seizure, and focal seizures may cause symptoms mimicking TIA. Stereotyped symptoms typically suggest seizures

Syncope (Chapter 6)

Loss of consciousness/blackouts is uncommon in TIA but can occur in posterior circulation TIAs with abrupt onset without prodrome. Accompanying brainstem symptoms are helpful in discriminating TIA from syncope

Previous stroke with intercurrent illness

Patients with cerebral damage from previous stroke frequently have recurrence of their stroke symptoms when systemically unwell, for example due to infection

Vestibular disorders

Can cause vertigo of abrupt onset mimicking vertebrobasilar TIA

Functional symptoms

Deficit (e.g. hemiparesis) without organic illness is uncommon

Pressure palsies (radial nerve palsy)

Differentiate using history from TIA

STROKE I: THROMBOEMBOLIC STROKE AND SYNDROMES

14

59

Stroke I: Thromboembolic stroke and syndromes

A stroke is a neurological deficit (usually focal but sometimes global) of cerebrovascular cause that persists beyond 24 h or leads to death within 24 h.

DEFINITION

EPIDEMIOLOGY Stroke is the third largest cause of death and the largest cause of severe disability in the United Kingdom and the United States. Around 150 000 people have a stroke each year in the United Kingdom; at any one time, over 300 000 people have moderate to severe disability because of stroke. Age-specific incidence of first-ever stroke in the United Kingdom is shown in Table 14.1. More than three-quarters of firstever strokes occur in over 65 s. Approximately 90% of all strokes are ischaemic in origin (rather than haemorrhagic). Stroke incidence is higher in males at young ages and in females at older ages. The incidence of stroke in the United Kingdom is falling. AETIOLOGY The commonest causes of thromboembolic stroke, particularly in older patients, are as follows:
Large-artery atherosclerosis (internal carotid, vertebral, basilar, aorta and middle cerebral arteries).
Cardioembolism, for example from atrial fibrillation, and left ventricular aneurysm.
Small-vessel occlusion, causing lacunar stroke (see Section ‘Clinical Syndromes’).
Arterial dissection with embolism, especially internal carotid artery (look for Horner’s syndrome), and vertebral arteries (a common cause of stroke in young patients, for example following minor neck trauma, and probably underrecognised in older patients, in whom one of the above causes may be presumed). Among the less common causes of stroke (mostly young onset) are the following:
Patent foramen ovale (PFO) with paradoxical embolism from venous thrombosis.
Antiphospholipid syndrome.
Vasculitis (usually young onset except giant cell arteritis).

Table 14.1 Total incidence of stroke (males and females) in the OXVASC study, Oxford, UK Age (years)

Incidence per 1000 population

F), increasing age (above 50–55 years of age), race (more common in African-Americans) and alcohol and drug abuse. Include questions specifically directed towards ascertaining the presence of any of the aetiological factors as above.

ASSOCIATIONS/RISK FACTORS

Spontaneous ICH usually occurs secondary to rupture of small penetrating vessels into brain parenchyma in basal ganglia, thalamus, pons or cerebellum, related to small vessel disease due to hypertension. Chronic hypertension causes degenerative changes within blood vessels and formation of microaneurysms of Charcot–Bouchard, occurring principally at bifurcation points of small perforating branches of lenticulostriate arteries (branch of middle cerebral artery) in basal ganglia. Clinical signs and subsequent deterioration is related to direct injury to brain from haemorrhage and further damage due to mass effect, hydrocephalus and increased intracranial pressure.

PATHOLOGY/PATHOGENESIS

Symptoms of raised intracranial pressure (see Chapter 30) with a focal neurological deficit (see below).

HISTORY

EXAMINATION Focal neurological deficits associated with spontaneous ICH may have a progressive onset, usually over minutes, unlike thromboembolic episodes which have a maximal deficit at the onset. Common sites are deep structures, including basal ganglia (50%) and thalamus (15%), pons (10%), cerebellum (10%) and cerebral hemispheres (lobar) (10–20%). Haemorrhage in the putamen, thalamus, pons and cerebellum are typically linked to hypertension. Clinical findings based on location are as follows:  Putaminal: Commonest site for ICH, causes contralateral hemiparesis or hemiplegia with conjugate deviation of the eyes ipsilateral to the side of the haematoma.

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CONDITIONS: APPLYING THE BASICS



Thalamic: Classically characterised by contralateral hemisensory loss or changes with dominant thalamic involvement also causing dysphasia. Small unreactive pupils with vertical gaze palsy with midbrain involvement.  Cerebellar: Can rapidly lead to clinical deterioration and coma as a result of direct brainstem compression or hydrocephalus from either the compression or the extension of haemorrhage into the fourth ventricle. Signs of cerebellar dysfunction (see Chapter 3).  Pontine: Coma with pinpoint unreactive pupils, quadriparesis or quadriplegia and respiratory disturbances, often fatal.  Lobar (see Chapter 3 for lobar syndromes). INVESTIGATIONS  Routine blood tests:

FBC (including platelet count), U & E (check for evidence of end organ damage related to hypertension and hyponatraemia related to SIADH), LFT, G & S, clotting profile (PT, APTT, and INR).  ECG: Look for evidence of left ventricular hypertrophy.  Imaging:  CT: Initial diagnostic investigation of choice, can be done rapidly and shows blood as high density (brighter) compared to brain parenchyma immediately after the event, shows degree of midline shift and mass effect, presence of associated intraventricular extension with or without hydrocephalus (Figure 15.1).  MRI: Useful at a delayed interval for demonstrating underlying structural abnormalities, for example a tumour.

Figure 15.1 CT demonstrates ICH in right temporal lobe with mass effect and effacement of ipsilateral frontal horn of right lateral ventricle.

STROKE II: INTRACEREBRAL HAEMORRHAGE

67

 Cerebral angiography: Generally recommended unless patients are above 45 years of age with known hypertension and have haemorrhage in putamen or thalamus. An angiogram should not delay the initial emergency treatment if required and can be performed at a delayed interval to increase the diagnostic yield. Remember: CT head is the initial diagnostic investigation of choice in ICH.

MANAGEMENT

Non-surgical Remember that adequate attention to airways and breathing and circulation (ABC) and securing of airway is particularly required in patients with low GCS (8). 

Hypertension: Slowly reduce blood pressure to patients’ premorbid levels if known; if not, aim for a 20% reduction in BP. Too rapid a correction, particularly in the presence of raised intracranial pressure, could lead to hypoperfusion and infarction. In initial stages, most patients with ICH will present with high BP irrespective of presence of premorbid hypertension due to increased ICP.  Correct any coagulopathy and stop any anticoagulant or antiplatelet medications. The following agents may be considered: fresh frozen plasma (coagulopathy), vitamin K and prothrombin complex concentrate (PCC) for warfarin; protamine sulphate for unfractionated heparin; platelet transfusion for patients with thrombocytopenia (12 h after headache onset.  CSF shows uniform blood staining in the first and third bottles with a xanthochromic (straw coloured) supernatant.  Confirmation of blood breakdown products is usually confirmed on CSF spectrophotometry which identifies the presence of CSF bilirubin if SAH has occurred.  If the patient is unconscious or with focal signs, an immediate neurosurgical referral is indicated without lumbar puncture. 

STROKE III: SUBARACHNOID HAEMORRHAGE

71

Figure 16.1 Axial CT Head showing acute subarachnoid blood (white) in right sylvian fissure, interhemispheric fissure and basal cisterns following rupture of an anterior communicating artery aneurysm.

MRI head:  For patients with delayed presentation, MRI has a high sensitivity for detecting subarachnoid blood.  Not helpful acutely (particularly